Jove
Visualize
お問い合わせ
JoVE
x logofacebook logolinkedin logoyoutube logo
JoVEについて
概要リーダーシップブログJoVEヘルプセンター
著者向け
出版プロセス編集委員会範囲と方針査読よくある質問投稿
図書館員向け
推薦の声購読アクセスリソース図書館諮問委員会よくある質問
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experimentsアーカイブ
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教員リソースセンター教員サイト
利用規約
プライバシーポリシー
ポリシー

関連する概念動画

Gallbladder01:17

Gallbladder

2.8K
The gallbladder is a small, pear-shaped organ that plays a crucial role in our digestive system. Measuring about 10 cm in length, it is comparable in size to a kiwi fruit and is located in a hollow area on the lower surface of the liver. The gallbladder's primary function is to store and concentrate bile, a fluid produced by the liver that aids in digestion.
The gallbladder's anatomy consists of three regions: the fundus, body, and neck. Extending from the neck, the cystic duct joins...
2.8K
Gastritis-I: Introduction and Types01:27

Gastritis-I: Introduction and Types

3.2K
Gastritis, defined by the inflammation or irritation of the stomach lining or gastric mucosa, manifests in several distinct forms: acute, chronic, reactive, and a specific subtype known as autoimmune metaplastic atrophic gastritis.
Acute gastritis presents as a sudden inflammation triggered by various stressors to the stomach lining, such as exposure to corrosive agents, local irritants like aspirin and other NSAIDs, alcohol consumption, radiation therapy, physical trauma, severe burns, sepsis,...
3.2K
Genome-wide Association Studies-GWAS01:11

Genome-wide Association Studies-GWAS

16.5K
Genome-wide association studies or GWAS are used to identify whether common SNPs are associated with certain diseases. Suppose specific SNPs are more frequently observed in individuals with a particular disease than those without the disease. In that case, those SNPs are said to be associated with the disease. Chi-square analysis is performed to check the probability of the allele likely to be associated with the disease.
GWAS does not require the identification of the target gene involved in...
16.5K
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

1.7K
Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
1.7K
Gastritis III: Clinical Manifestations and Management01:23

Gastritis III: Clinical Manifestations and Management

1.6K
The clinical manifestations of gastritis can vary depending on the cause and type of gastritis, but some common symptoms may include the following.
Clinical manifestations of acute gastritis
The patient with acute gastritis may have a rapid onset of symptoms, such as epigastric pain or discomfort, dyspepsia, anorexia, hiccups, or nausea and vomiting, which can last from a few hours to a few days. Erosive or hemorrhagic gastritis may cause bleeding, which may manifest as blood in vomit or as...
1.6K
Adrenal Gland Disorders01:27

Adrenal Gland Disorders

3.8K
Adrenal gland disorders manifest when the production of adrenal hormones deviates from the norm, resulting in either excessive or insufficient concentrations.
Adrenal insufficiency, characterized by insufficient cortisol and aldosterone production, leads to conditions like Addison's disease. This disorder, affecting the adrenal cortex, exhibits symptoms such as skin bronzing, dehydration, low blood pressure, fatigue, and weight loss. Congenital adrenal hyperplasia, a genetic ailment causing...
3.8K

こちらも読む

関連記事

共著者、ジャーナル、引用グラフによってこの研究に関連する記事。

並び替え
Same author

Anti-neutrophil cytoplasmic antibody associated vasculitis: a retrospective epidemiological study in an Aotearoa New Zealand cohort.

The New Zealand medical journal·2026
Same author

A Return to Normality: A Descriptive Qualitative Interview Study Exploring the Patient Experience of Gout Flare Resolution.

Arthritis care & research·2026
Same author

Musculoskeletal ultrasound findings in people with asymptomatic hyperuricemia: baseline analysis from the Transitions in Gout Research (TIGER) study using the OMERACT gout ultrasound semiquantitative scoring system.

Annals of the rheumatic diseases·2026
Same author

Mitonuclear Discordance and Gout, Type 2 Diabetes and Chronic Kidney Disease in Aotearoa New Zealand Indigenous Māori and Pacific People.

Annals of human genetics·2026
Same author

Revisiting the Ethics of Urate-Lowering Therapy Clinical Trials for Gout Management.

Arthritis & rheumatology (Hoboken, N.J.)·2026
Same author

Misclassified latent autoimmune diabetes in adults within Māori and Pacific adults with type 2 diabetes in Aotearoa New Zealand.

The New Zealand medical journal·2025
Same journal

Inherited retinal degenerations: clinical phenotypes and emerging therapies.

Lancet (London, England)·2026
Same journal

Documenting hospice care.

Lancet (London, England)·2026
Same journal

After the wood chipper.

Lancet (London, England)·2026
Same journal

Assisted dying and the silencing of medicine's next generation.

Lancet (London, England)·2026
Same journal

Linguistic pragmatism: a woman with progressive abdominal pain in Thailand.

Lancet (London, England)·2026
Same journal

Medical compartmentalisation: a patient with chromosome 22q11.2 deletion syndrome in Japan.

Lancet (London, England)·2026
関連記事をすべて見る

関連する実験動画

Updated: Mar 22, 2026

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
06:35

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis

Published on: February 8, 2019

7.9K

痛風

Nicola Dalbeth1, Tony R Merriman2, Lisa K Stamp3

  • 1Department of Medicine, University of Auckland, Auckland, New Zealand.

Lancet (London, England)
|April 27, 2016
PubMed
まとめ
この要約は機械生成です。

効果的な痛風管理には,血清ウラート濃度を360μmol/L以下に低下させる必要があります. アロピュリノールのような治療法があるにもかかわらず,尿酸を下げる治療の開始および継続率は低いため,発症抑制が困難です.

さらに関連する動画

Quantitative SERS Detection of Uric Acid via Formation of Precise Plasmonic Nanojunctions within Aggregates of Gold Nanoparticles and Cucurbit[n]uril
10:02

Quantitative SERS Detection of Uric Acid via Formation of Precise Plasmonic Nanojunctions within Aggregates of Gold Nanoparticles and Cucurbit[n]uril

Published on: October 3, 2020

4.6K
The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis
11:39

The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis

Published on: July 11, 2013

39.6K

関連する実験動画

Last Updated: Mar 22, 2026

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
06:35

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis

Published on: February 8, 2019

7.9K
Quantitative SERS Detection of Uric Acid via Formation of Precise Plasmonic Nanojunctions within Aggregates of Gold Nanoparticles and Cucurbit[n]uril
10:02

Quantitative SERS Detection of Uric Acid via Formation of Precise Plasmonic Nanojunctions within Aggregates of Gold Nanoparticles and Cucurbit[n]uril

Published on: October 3, 2020

4.6K
The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis
11:39

The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis

Published on: July 11, 2013

39.6K

科学分野:

  • リウマトロジ
  • クリスタル誘発性関節炎
  • 免疫学

背景:

  • 痛風は,血清ウラートの高さによる単酸ナトリウム結晶の堆積によって引き起こされる慢性疾患です.
  • 腎臓と腸内尿酸の排泄が重要な調節メカニズムである.
  • NLRP3炎症体の活性化とインタールキン-1βの放出は,急性痛風の発症に不可欠です.

研究 の 目的:

  • 効果的な痛風管理のための"血清ウラートへの治療"戦略の重要性を強調する.
  • 結晶溶解と発火抑制のための長期の血清ウラート減少の目標を強調する.
  • 痛風の治療の質を改善する戦略の必要性を特定する.

主な方法:

  • 結晶形成と炎症経路を含む痛風の病理学に関する現在の理解をレビューする.
  • アロピュリノールの投与量エスカレーションや新しい尿酸低下薬を含む治療方法の検討
  • 尿酸を下げる治療の開始率と継続率の世界的な傾向の分析

主要な成果:

  • 血清尿酸の目標値 (<360μmol/ L) を達成することは,結晶の溶解と発症抑制につながる痛風の管理に不可欠です.
  • アロプーリノールの投与量を増やすことはしばしば効果的であり,新しい尿酸低下薬が利用可能である.
  • 世界的に,尿酸を下げる治療の開始と遵守は不適正であり,治療目標の達成はまれである.

結論:

  • 痛風を効果的に管理するには"血清尿酸を標的とする治療法"が不可欠です.
  • 現在,尿酸を下げる治療の利用率が低いため,世界的に成功する痛風の管理が困難です.
  • 痛風の治療の質と 患者の治療順守を改善するために 強化された戦略が不可欠です